Exam 2 lecture 5 Flashcards

1
Q

steps for electrical conduction in heart

A
  1. SA node fires (pacemaker cells start beating)
  2. Excitation spreads through atrial myocardium
  3. AV node fire
  4. Excitation spreads down AV bundle
  5. Purkinje fibers distribute excitation through ventricular
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2
Q

PQRST meaning

A

P- beginning
Q- 1st dip
R- highest tip
S- Second dip
T- last beat

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3
Q

P wave is a culmination of

A

SA node, atrium and AV node

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4
Q

QT is determined by

A

Wide action potential mediated by Ca2+

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5
Q

What are some important ion channels in heart

A

Na channels
Calcium channels
K channels
HCN channels
hERG channels

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6
Q

What are the types of Na, Ca, K, HCN and hERG channels in heart

A

Na- Na V 1.5
Ca- N type, CaV 2.2, T type
K- Kir, Kv
HCN- HCN1, HCN 4
hERG- KCNH2, KV 11.1

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7
Q

what is an important channel to avoid targeting when developing new drugs

A

hERG

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8
Q

Membrane concentration of cells inside and outside of cells

A

inside
K- more K inside
Na- less Na inside
Ca- less Ca inside
Cl- less Cl inside

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9
Q

charge inside the cell vs outside the cell numerical value

A

inside- -70mV
outside- 0 mV

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10
Q

explain how an action potential is formed

A

-Na channels open and cause depolarization
-causes a rise in membrane potential
-Na channels close and there is a plateu when Ca cells come into cell and K cells go out of cell (cause contration)
- when Ca channel closes, rapid repolarization occurs

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11
Q

compare pacemaker cells and ventricular myocytes (important)

A

pacemaker cells
-specialized non-contractile cells
-physiologically depolarized
-Ca2+ dependent spikes
ACTION POTENTIAL -50mV
no plateu in image

Ventricular myocytes
- contractile cells
-hyperpolarized
-Na2+ dependent spikes
-86 mV action potential
long plateu phase

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12
Q

how does Ach affect Ca and HCN

A

reduce both

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13
Q

how does Ach affect ion channels

A

cause hyperpolarization and block activation of ion channels (reduce HR)

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14
Q

what are the 3 phases of Na channels in phase 0

A

Rest
open
inactivation

during rest- flat on graph
Open makes it shoot up
inactivation (ball and chain method ball plugs hole) causes a slow decline to rest)

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15
Q

can we form another action potential when channel is inactivated

A

no, it is called the refractory period

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16
Q

phase 2 and 3 of action potential generation

A

K+ channel opens and drives K out
Ca channel brings Ca inside
This causes a plateau
eventually ca channels will be inactivated then most of the force will be mediated by K channels, action potential goes down

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17
Q

Re entry arrhythmia requirements

A
  1. multiple parallel pathway
  2. Unidirectional block
  3. conduction time greater than ERP (effective refractory period)
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18
Q

What are the Antiarrhythmic drugs

A

Class 1- Na channel blockers
Class 2- B adrenergic antagonists
Class 3- K channel blockers (prolong refractory period)
Class 4 Caclium channel blockers

19
Q

Which 2 classes of antiarrhythmic drugs have common features

A

Class 2 and 4 (B adrenergic and Ca2+)

20
Q

Know the difference in how class 2 and class 4 look in EKG

A

Class 2 peaks have the same height
view notebook
CCB causes reduction in peak

21
Q

How do B adrenergic agonists affect HR

A

slow it down

22
Q

how do class 2 anti arrhythmics (BAR blockers) affect pacemakers? Ca currents? PR interval? refractoriness of AV node?

A

slow pacemakers
slow Ca currents
increase PR interval
increase refractoriness of AV node

23
Q

are class IV anti arrythmics (CCBs) frequency dependent blocks

24
Q

How do class IV antiarrythmics affect refractoriness of AV node? PR interval? ventricular rate?

A

increase refractoriness of AV node
protects ventricular rate from tachycardia

25
What are some BAR drugs used as antiarrythmics? are they cardio selective or non selective
Esmolol (cardioselective) acebutolol (cardioselective) propranolol(non-selective)
26
Know the structure of esmolol for exam
27
clinical use of BAR drugs
arrhythmias involving catecholamines
28
What are the Class IV (CCB) drugs
Verapamil Diltiazem
29
use of diltiazem as antiarrhythmic
Block re-entrant arrhythmias involving AV node
30
how to recognize diltiazem and verapamil structures
verapamil- has double oxygen on left and right side Diltiazem- has N and S in structure Google structure
31
What are the different types of Class 1 antiarrhythmic drugs
Class 1A- Mixed block (Na and K) Class 1B- Na channel blocker Class 1C- Strong Na blocker
32
What are the different 1A, 1B and 1C drugs
1A- Quinidine, procainamide 1B- lidocaine, mexiletine 1C- Flecainide, propafenone
33
Class 1A drug effect on action potential
Widen QRS and prolong QT
34
Class 1B drug effect on action potential
Has no clinical significance on ECG
35
Class 1C effect on action potential
Widen QRS
36
Which states of Na do 1A, 1B and 1C drugs affect
Class 1A- blocks open state Class 1B- Blocks open and inactive state Class 1C- Blocks open state
37
Class III anti arrythmics MOA
K channel blockers
38
How do class III antiarythmics effect ECG
prolong action potential duration and QT interval increase ERP
39
class III drug name
Amiodarone dronedarone sotalol
40
why is amiodarone important
top choice for rate control in A fib, suppression of post MI ventricular arrythmia
41
What are acquired long QT syndromes
Genetic mutations (KCNQ1 (potassoum) SCNSA (sodium) cause LQTS
42
where do different classes of antiarrythmics affect the action potential
Class 1 affects the first rise (depolarization) Class 4 affects the plateau Class 3 affects the repolarization (down graph) Class 2 affects the very end
43
what are some miscellaneous antiarrythmic drug
Digoxin Adenosine (leads to slowing of heart)